Abstract
ObjectiveTo evaluate the immunological profile and gene expression of endothelin-1 (ET-1) in mitral valves of patients with rheumatic fever originated from a reference service in cardiovascular surgery.MethodsThis was a quantitative, observational and cross-sectional study. Thirty-five subjects (divided into four groups) participated in the study, 25 patients with chronic rheumatic heart disease and ten control subjects. The mean age of the sample studied was 34.5 years. Seventeen of them (48.58%) were male and 18 (51.42%) were female. Inflammatory cytokines (TNF-α, IL-4 and IL-10) were measured and ten mitral valves of patients who underwent first valve replacement were collected for determination of gene expression of endothelin-1 by real time PCR.ResultsAmong the groups studied (patients vs. controls), there was a statistically significant difference in IL-10 levels (P=0.002), and no differences in other cytokines. Expression of endothelin-1 was observed in 70% of samples. Quantitatively, average of ET-1 expression was 62.85±25.63%.ConclusionInflammatory cytokine IL-10 participates in the maintenance of chronicity of rheumatic fever in patients who underwent valve replacement and those who are undergoing medical treatment. The expression of endothelin-1 in heart valve lesions in patients undergoing mitral valve replacement confirms its association with inflammatory activity in rheumatic fever.
Highlights
Rheumatic fever (RF) represents a serious public health problem
This leads to production of inflammatory cytokines (e.g., TNF-α, IL-2, and IL-10), which have a decisive influence on the immune response of patients with rheumatic fever
Serum levels of TNF-alpha as well as the levels of IL-4 and IL-10 were shown to be reduced when compared to a previous study [20]
Summary
Rheumatic fever (RF) represents a serious public health problem It is a rheumatic and inflammatory disease of autoimmune origin, which occurs in response to an infection by group A streptococcus (Streptococcus pyogenes). Studies indicate that the inflammatory response in acute RF on cardiac tissues is generated by antigenic mimicry of the protein M leading to an abundant infiltration of CD4+ T cells [5,6,7]. This leads to production of inflammatory cytokines (e.g., TNF-α, IL-2, and IL-10), which have a decisive influence on the immune response of patients with rheumatic fever. It is known that increased levels of Th1 inflammatory cytokines (TNF-α and IFN-γ) and lower levels of Th2 and regulatory cytokine IL-4 lead to maintenance and progression of rheumatic valvulopathy [8,9,10,11,12]
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